From: BACE1 inhibitor drugs in clinical trials for Alzheimer’s disease
Phenotype | Putative Substrate | References |
---|---|---|
Astrogenesis increase; neurogenesis decrease | Jag1 | [46] |
Axon guidance defects | CHL1 | |
Hyperactivity | NRG1 | |
Hypomyelination | NRG1 | |
Memory deficits | Unknown | |
Insulin sensitivity enhanced | Unknown | |
Muscle spindle reduction | NRG1 | [44] |
Neurochemical deficits | Unknown | [45] |
Neurodegeneration with age | Unknown | [47] |
Postnatal lethality, growth retardation | Unknown | [29] |
Retinal abnormalities | VEGFR1 | [49] |
Schizophrenia endophenotypes | NRG1 | [48] |
Seizures | Navβ2 | |
Spine density reduction | NRG1 | [48] |
BACE2 knockout mouse phenotypes | ||
Phenotype | Putative Substrate | References |
Normal | --- | [29] |
Pancreatic β cell increase | Tmem27 | [54] |
Pigmentation abnormalities | PMEL | [55] |
BACE1/2 double knockout mouse phenotypes | ||
Phenotype | References | |
Similar to BACE1 knockout, except postnatal lethality is enhanced | [29] |